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Abstract: FR-PO059

Neonatal AKI in a Juvenile Rabbit Model Results in Reduced Nephron Number Assessed by MRI

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Charlton, Jennifer R., University of Virginia, Charlottesville, Virginia, United States
  • Baldelomar, Edwin, University of Hawaii at Manoa, Honolulu, Hawaii, United States
  • Nam, Sejin, University of Hawaii at Manoa, Honolulu, Hawaii, United States
  • Bennett, Kevin M., University of Hawai'i, Honolulu, Hawaii, United States

Acute kidney injury (AKI) affects 30% of preterm neonates. Preterm neonates develop AKI during nephrogenesis conferring a risk for chronic kidney disease. Current monitoring practices cannot detect microstructural changes in the kidney. Our objective was to assess if the renal microstructure, number (Nglom) and volume (Vglom) of the glomeruli, is affected by AKI during nephrogenesis using cationic ferritin enhanced MRI (CFE-MRI).


New Zealand rabbits were used as nephrogenesis occurs for 3 postnatal weeks. The AKI group received indomethacin and gentamicin at week #1 for four days. At six weeks, the AKI and control groups (5/grp) were injected with cationic ferritin, euthanized and kidneys were imaged (7T ClinScan GRE pulse sequence:TR:80/TE:20, thickness 0.17, FOV 29, 448*448 matrix, FA 25o). Nglom and Vglom were determined by threshold guiding with a watershed transformation.


Body and kidney weights were significantly lower in the AKI group. The kidney/body weight and renal function measured by serum creatinine was not different between the groups. Nglom and Vglom were lower in the AKI group (Nglom: 86387 vs 178093, p=0.01; Vglom: 319044 vs. 425029 μm3, p=0.01), Fig 1. AKI kidneys had a layer of glomeruli which were not labeled and undetectable by MRI. On histological assessment, the glomeruli in the undetectable region were shrunken, immature and lacked tubules (Fig 2).


Neonatal AKI from gentamicin and indomethacin causes permanent glomerular reduction without glomerular hypertrophy. Tools such as CFE-MRI that allow us to visualize and quantify renal microstructure to detect early CKD and evaluate the nephrotoxic potential of medications during nephrogenesis.


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